Thrombospondin-1 in vascular development, vascular function, and vascular disease

• Published in: Seminars in cell & developmental biology Vol. 155; no. Pt B; pp. 32 - 44
• Main Authors: Liu, Bo, Yang, Huan, Song, Yong-Seok, Sorenson, Christine M., Sheibani, Nader
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.03.2024
• Subjects: Abdominal aortic aneurysm; Angiogenesis; Cell adhesion; Cell migration; Extra cellular matrix; Humans; Neoplasms - pathology; Neovascularization, Pathologic - pathology; Ocular neovascularization; Vascular cells; Vascular Diseases; CCL5/RANTES; CFH; RPE; PC/SMC; TSP1; cGMP; CNS; CNV; Angiogenesis; CCL2/MCP-1; Cell adhesion; NG2; PDGFR; EC; AAA; Alk-1; AC; AD; VEGF; Abdominal aortic aneurysm; BMP9; PAX2; RGC; Ocular neovascularization; PDGF; TGFβ; OIR; Cell migration; Vascular cells; Extra cellular matrix
• ISSN: 1084-9521; 1096-3634; 1096-3634
• DOI: 10.1016/j.semcdb.2023.07.011

Angiogenesis is vital to developmental, regenerative and repair processes. It is normally regulated by a balanced production of pro- and anti-angiogenic factors. Alterations in this balance under pathological conditions are generally mediated through up-regulation of pro-angiogenic and/or downregulation of anti-angiogenic factors, leading to growth of new and abnormal blood vessels. The pathological manifestation of many diseases including cancer, ocular and vascular diseases are dependent on the growth of these new and abnormal blood vessels. Thrompospondin-1 (TSP1) was the first endogenous angiogenesis inhibitor identified and its anti-angiogenic and anti-inflammatory activities have been the subject of many studies. Studies examining the role TSP1 plays in pathogenesis of various ocular diseases and vascular dysfunctions are limited. Here we will discuss the recent studies focused on delineating the role TSP1 plays in ocular vascular development and homeostasis, and pathophysiology of various ocular and vascular diseases with a significant clinical relevance to human health.